Lecture 18 - Treatment of Diabetes Mellitus (DM)

‭Diabetes Mellitus‬ ‭●‬ ‭Primarily a disorder of carbohydrate metabolism‬ ‭○‬ ‭Also disrupts metabolism of proteins and lipids‬ ‭●‬ ‭Type I diabetes‬ ‭○‬ ‭Usually childhood/adolescent onset due to decreased ability to make insulin‬ ‭○‬ ‭Destruction of pancreatic beta cells, which produce insulin‬ ‭○‬ ‭Autoimmune process; sudden onset‬ ‭●‬ ‭Type II diabetes‬ ‭○‬ ‭Most commonly develops middle-age‬ ‭○‬ ‭Gradual progression; still able to perfuse insulin‬ ‭○‬ ‭Insulin resistance due to decreased affinity and receptor numbers‬ ‭○‬ ‭Impaired insulin secretion‬ ‭Diagnosis of DM‬ ‭●‬ ‭Fasting blood sugar (FBS) ≥ 126 mg/dL‬ ‭○‬ ‭Normal 80-109 mg/dL‬ ‭●‬ ‭Random blood sugar (RBG) ≥ 200 mg/dL‬ ‭●‬ ‭Oral glucose tolerance test (OGTT) ≥ 200 mg/dL‬ ‭○‬ ‭OG load given and plasma glucose is measured later‬ ‭○‬ ‭Usually tested in women for gestational diabetes‬ ‭●‬ ‭Hemoglobin A1C ≥ 6.5%‬ ‭○‬ ‭Gold standard; long-term management‬ ‭○‬ ‭Glucose binds to Hgb (glycolysated)‬ ‭○‬ ‭Normally 4-5.6%, but results affected by Hgb levels/disorders‬ ‭○‬ ‭Reflects glucose control over 2-3 month period‬ ‭Increased Health Risks of DM/Chronic Hyperglycemia‬ ‭●‬ ‭CVD: HTN, stroke‬ ‭●‬ ‭Retinopathy‬ ‭●‬ ‭Renal failure‬ ‭●‬ ‭Painful neuropathy‬ ‭●‬ ‭Diabetic foot ulcedration‬ ‭●‬ ‭Lower extremity amputations; decreased sensation‬ ‭Classification of DM‬ ‭●‬ ‭Type I DM: Insulin-dependent‬ ‭●‬ ‭Type II DM: Treatments vary‬ ‭○‬ ‭If insulin-resistant (pre-diabetic), may be controlled with diet/exercise‬ ‭○‬ ‭Oral agents‬ ‭○‬ ‭Insulin‬ ‭●‬ ‭Gestational diabetes mellitus (GDM)‬ ‭○‬ ‭Some oral agents‬ ‭○‬ ‭May be insulin-dependent‬ ‭Assessment Findings‬ ‭●‬ ‭3 Ps: Polyuria, polydipsia, polyphagia‬ ‭●‬ ‭Fatigue‬ ‭●‬ ‭Body weakness‬ ‭●‬ ‭Visual changes‬ ‭●‬ ‭Slow wound healing‬ ‭●‬ ‭Recurrent infections (ex. Yeast, skin)‬ ‭Nursing Management‬ ‭●‬ ‭Goal: Normalize insulin activity and blood‬ ‭glucose levels‬ ‭●‬ ‭Dietary management‬ ‭●‬ ‭Routine exercise‬ ‭●‬ ‭Consistent glucose monitoring‬ ‭●‬ ‭Drug therapy‬ ‭●‬ ‭Patient education‬ ‭Drug Therapy: Insulin‬ ‭●‬ ‭Therapeutic goal: To have the right amount‬ ‭of insulin available to the cells when glucose‬ ‭is available; match what the body produces‬ ‭●‬ ‭Glucose stimulates the production of insulin‬ ‭Therapeutic Benefits of Insulin Therapy‬ ‭●‬ ‭Promotes energy conservation‬ ‭●‬ ‭Builds glucose stores‬ ‭●‬ ‭Stimulates uptake of glucose into cells‬ ‭●‬ ‭Promotes synthesis of larger molecules‬ ‭○‬ ‭Glucose → glycogen‬ ‭○‬ ‭Amino acids →‬‭proteins‬ ‭○‬ ‭Fatty acids → triglycerides‬ ‭○‬ ‭Reverse occurs in DM‬ ‭Categories of Insulin Therapy‬ ‭●‬ ‭Source: Recombinant DNA technology‬ ‭○‬ ‭Human: Equal to what the body would produce‬ ‭ ‬ ‭Analogs: Modified human insulin‬ ○ ‭ ‬ ‭Onset/duration of action:‬ ● ‭○‬ ‭Short-duration/rapid-acting‬ ‭○‬ ‭Short-duration/short-acting‬ ‭○‬ ‭Intermediate-duration/slow-acting‬ ‭○‬ ‭Long-duration/slow-acting‬ ‭●‬ ‭Concentration:‬ ‭○‬ ‭100 u/mL (most common)‬ ‭○‬ ‭200 u/mL‬ ‭○‬ ‭300 u/mL‬ ‭○‬ ‭400 u/mL‬ ‭○‬ ‭500 u/mL‬ ‭Time-Effect of Insulin (sub-Q)‬ ‭Complications of Insulin Use‬ ‭●‬ ‭Hypoglycemia (BG level < 70 mg/dL)‬ ‭○‬ ‭Medication error (overcorrection)‬ ‭○‬ ‭Change in intake/exercise‬ ‭○‬ ‭Illness (vomiting/diarrhea)‬ ‭■‬ ‭Loss > intake‬ ‭●‬ ‭Hypokalemia: Overcorrection of hyperkalemia‬ ‭●‬ ‭Allergic reaction: Lower risk‬ ‭●‬ ‭Drug interactions:‬ ‭○‬ ‭Hypoglycemic agents (ex. Oral agents such as sulfonylureas and glinides)‬ ‭○‬ ‭Alcohol: Lowers glucose levels‬ ‭‬ H ○ ‭ yperglucemic agents: Increased insulin‬ ‭○‬ ‭Beta-blockers: Mask the S/S of hypoglycemia‬ ‭Patient Education‬ ‭●‬ ‭Insulin administration (sub-Q)‬ ‭●‬ ‭Self-monitoring glucose‬ ‭●‬ ‭S/S of hyperglucemia‬ ‭●‬ ‭S/S of ketoacidosis‬ ‭●‬ ‭S/S of hypoglycemia‬ ‭Insulin Administration‬ ‭●‬ ‭Insulin is absorbed fastest in the abdomen and‬ ‭slowest in the hips‬ ‭○‬ ‭May cause variation in onset‬ ‭●‬ ‭Rotate the areas of injection to avoid‬ ‭lipohypertrophy (accumulated sub-Q fat)‬ ‭●‬ ‭Cleanse the skin prior (alcohol or soap and water)‬ ‭●‬ ‭Inject at a 45-90 degree angle‬ ‭●‬ ‭Proper storage and disposal of needles‬ ‭Injection Devices‬ ‭●‬ ‭Use a syringe that matches the units being given‬ ‭●‬ ‭Smallest needle is often used in pediatrics‬ ‭●‬ ‭1 mL: U100‬ ‭●‬ ‭½ mL: U50‬ ‭●‬ ‭⅓ mL: U30‬ ‭Self-Monitoring Glucose‬ ‭●‬ ‭Allows individual to adjust treatment regimen and obtain optimal glucose control‬ ‭●‬ ‭Common method: Capillary blood on test strip‬ ‭●‬ ‭Frequency varies, up to 8 times a day‬ ‭●‬ ‭When it is done:‬ ‭ ‬ ‭Basal level: Before meals (< 180 mg/dL)‬ ○ ‭○‬ ‭Postprandial (> 180 mg/dL)‬ ‭○‬ ‭Peak action time of medication to evaluate need for adjustment‬ ‭○‬ ‭Bedtime‬ ‭ ‬ ‭Continuous monitoring is done every 5 minutes; prevents hypoglycemia episodes‬ ● ‭Symptoms of Hyperglycemia‬ ‭●‬ ‭Fatigue‬ ‭●‬ ‭Blurry vision‬ ‭●‬ ‭Polydipsia‬ ‭●‬ ‭Fruity breath‬ ‭●‬ ‭Polyphagia‬ ‭●‬ ‭N/V‬ ‭●‬ ‭Polyuria‬ ‭Diabetic Ketoacidosis‬ ‭●‬ ‭Occuts with uncontrolled hyperglycemia‬ ‭●‬ ‭Without insulin, glucose is unable to enter cells‬ ‭●‬ ‭Body begins breaking down fat for energy‬ ‭●‬ ‭Process produces a build-up of acids (ketones), creating metabolic acidosis‬ ‭●‬ ‭Fruity breath often observed‬ ‭●‬ ‭Can be fatal if untreated due to low glucose serum levels‬ ‭○‬ ‭Treatment is IV‬ ‭Symptoms of Acidosis‬ ‭●‬ ‭Headache‬ ‭●‬ ‭Drowsiness, coma‬ ‭●‬ ‭Coma, loss of consciousness‬ ‭●‬ ‭Seizures, weakness‬ ‭●‬ ‭Diarrhea‬ ‭●‬ ‭SOB, coughing‬ ‭●‬ ‭Arrythmias, tachycardia‬ ‭●‬ ‭N/V‬ ‭Symptoms of Hypoglycemia‬ ‭●‬ ‭Shaking or tremors‬ ‭●‬ ‭Tachycardia, anxiety, panic‬ ‭●‬ ‭Hunger‬ ‭●‬ ‭Mouth tingling‬ ‭●‬ ‭Sweating‬ ‭ ‬ ‭Headache, inability to concentrate‬ ● ‭●‬ ‭Nausea‬ ‭●‬ ‭Dizziness and weakness‬ ‭Treatment of Severe Hypoglycemia: Glucagon‬ ‭●‬ ‭MOA: Increases blood sugar levels by promoting breakdown of glycogen to glucose‬ ‭○‬ ‭Stimulates biosynthesis of glucose‬ ‭●‬ ‭Used to treat severe hypoglycemia in ambulatory settings‬ ‭○‬ ‭Return to consciousness occurs within 20 minutes‬ ‭●‬ ‭Preferred inpatient treatment is IV glucose‬ ‭●‬ ‭Immediate treatment would be to ingest sugar‬ ‭Short-Duration/Rapid-Acting Insulin‬ ‭●‬ ‭Prototypes: Lispro (Humalog), Insulin Aspart (Novolog), Glulisine (Apidra)‬ ‭●‬ ‭Rapid effect, short duration‬ ‭○‬ ‭Controls postprandial rise of glucose‬ ‭●‬ ‭Onset: About 10-20 minutes‬ ‭●‬ ‭Peak: 0.5-3 hours‬ ‭●‬ ‭Duration: 3-5 hours‬ ‭●‬ ‭Education: Patient should eat within 10-15 minutes after injection‬ ‭Short-Duration/Short-Acting Insulin‬ ‭●‬ ‭Prototype: Regular Insulin (Humulin R, Novolin R)‬ ‭●‬ ‭Controls postprandial rise in glucose‬ ‭●‬ ‭Administer: 30 minutes before a meal‬ ‭●‬ ‭Onset: 0.5-1 hour‬ ‭●‬ ‭Peak: 1-5 hours‬ ‭●‬ ‭Duration: 6-10 hours‬ ‭●‬ ‭Education: Patient should eat ~30 minutes after injection‬ ‭Intermediate-Duration/Action Insulin‬ ‭●‬ ‭Prototype: Neutral Protamine Hagedorn (NPH) Insulin Suspension (Humalin N),‬ ‭(Novolin N)‬ ‭○‬ ‭Distinct appearance: White and cloudy‬ ‭○‬ ‭All other insulins are clear and colorless‬ ‭●‬ ‭Use: Glycemic control in between meals and at night‬ ‭●‬ ‭Onset: 1-2 hours‬ ‭●‬ ‭Peak: 6-14 hours‬ ‭●‬ ‭Duration: 16-24 hours‬ ‭●‬ ‭Only longer-acting insulin suitable for mixing with short-acting‬ ‭●‬ ‭Patient education: Do not shake, not for postprandial hyperglycemia‬ ‭Long-Duration/Slow-Acting Insulin‬ ‭●‬ ‭Prototype: Glargine (Lantus), Detemir (Levemir)‬ ‭●‬ ‭Peakless insulin (basal insulin)‬ ‭●‬ ‭Onset: 1 hour‬ ‭●‬ ‭Peak: None‬ ‭●‬ ‭Duration: 18-24 hours‬ ‭●‬ ‭Patient education: Do not mix with other insulins, not for postprandial rise in glucose,‬ ‭give at the same time each day‬